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anti-Human LFNG Antibodies:
anti-Mouse (Murine) LFNG Antibodies:
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Human Polyclonal LFNG Primary Antibody for IHC (p), WB - ABIN953163
Dunwoodie: Mutation of the fucose-specific beta1,3 N-acetylglucosaminyltransferase LFNG results in abnormal formation of the spine. in Biochimica et biophysica acta 2009
Show all 2 references for ABIN953163
Cow (Bovine) Polyclonal LFNG Primary Antibody for WB - ABIN2782070
Sparrow, Chapman, Wouters, Whittock, Ellard, Fatkin, Turnpenny, Kusumi, Sillence, Dunwoodie: Mutation of the LUNATIC FRINGE gene in humans causes spondylocostal dysostosis with a severe vertebral phenotype. in American journal of human genetics 2005
Human Polyclonal LFNG Primary Antibody for ELISA, WB - ABIN1534692
Johnston, Rauskolb, Wilson, Prabhakaran, Irvine, Vogt: A family of mammalian Fringe genes implicated in boundary determination and the Notch pathway. in Development (Cambridge, England) 1997
TGFBR2 (show TGFBR2 Antibodies) signaling can affect Notch1 (show NOTCH1 Antibodies) glycosylation via regulation of glycosyltransferase (show GTDC2 Antibodies) LFNG expression and provide a first mechanistic example for altered glycosylation in microsatellite instability colorectal tumor cells.
LFNG expression correlates with expansion of cancer stem cell populations and NKX3.1 (show NKX3-1 Antibodies) expression in human prostate cancer.
Reduced LFNG expression facilitates JAG/NOTCH (show NOTCH1 Antibodies) luminal progenitor signaling and cooperates with MET/CAVEOLIN basal-type signaling to promote basal-like breast cancer.
Mutation of the LFNG gene causes spondylocostal dysostosis with a severe vertebral phenotype, reinforcing the hypothesis that proper regulation of the Notch (show NOTCH1 Antibodies) signaling pathway is an absolute requirement for the correct patterning of the axial skeleton.
Fringe modifications at EGF8 and EGF12 enhanced Notch1 binding to and activation from Delta-like 1, while modifications at EGF6 and EGF36 (added by Manic and Lunatic but not Radical) inhibited Notch1 activation from Jagged1.
LFNG protein may have context-dependent effects on Notch (show NOTCH1 Antibodies) activity; somitogenesis is disrupted by a novel dominant allele of Lfng
Lfng expression and activity is normal in mice whose Lfng is lengthened by 10 kb, and no effects on segmentation are evident.
suggest that modulation of the Notch (show NOTCH1 Antibodies) signaling by Lfng affects the clock period during development
STAT5 (show STAT5A Antibodies)-dependent amplification of Notch (show NOTCH1 Antibodies)-modifying Lfng augments Th2 response via Dll4 (show DLL4 Antibodies) and is critical for amplifying viral exacerbation during allergic airway disease.
The repressive effect of Lfng against Notch (show NOTCH1 Antibodies) activities in neighbouring cells can sufficiently explain the synchronization in vivo.
Intriguing changes are observed in the cranio-caudal (show CAD Antibodies) borders of multifidus muscle in mutant Dll3 (show DLL3 Antibodies) and Lfng models of idiopathic scoliosis.
the presence of Gal (show GAL Antibodies) on O-fucose glycans differentially affects DLL1 (show DLL1 Antibodies)-induced NOTCH (show NOTCH1 Antibodies) signaling modulated by LFNG versus MFNG (show MFNG Antibodies)
Decreasing Lfng expression during the (TCR-CD4 (show CD4 Antibodies)/CD8 (show CD8A Antibodies) double negative 3) DN3-DP (CD4 (show CD4 Antibodies)/CD8 (show CD8A Antibodies) double positive) transition minimizes the potent leukemogenic potential of Notch1 (show NOTCH1 Antibodies) signaling.
lfng regulates delta-notch (show NOTCH1 Antibodies) induction of hypochord.
The sequence and embryonic expression of lfng were studied.
Lfng acts in a feedback loop downstream of proneural genes.
This gene is a member of the fringe gene family which also includes radical and manic fringe genes. They all encode evolutionarily conserved glycosyltransferases that act in the Notch signaling pathway to define boundaries during embryonic development. While their genomic structure is distinct from other glycosyltransferases, fringe proteins have a fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that leads to elongation of O-linked fucose residues on Notch, which alters Notch signaling. This gene product is predicted to be a single-pass type II Golgi membrane protein but it may also be secreted and proteolytically processed like the related proteins in mouse and Drosophila (PMID: 9187150). Mutations in this gene have been associated with autosomal recessive spondylocostal dysostosis 3. Multiple transcript variants encoding different isoforms have been found for this gene.
, beta-1,3-N-acetylglucosaminyltransferase lunatic fringe
, O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase
, lunatic fringe gene homolog
, lunatic fringe homolog